Pancreatic cancer and Amplia Therapeutics

I was delighted to sit down with Dr Chris Burns, CEO of Amplia Therapeutics, to discuss narmafotinib, their oral FAK (focal adhesion kinase) inhibitor designed to improve chemotherapy in pancreatic ductal adenocarcinoma/PDAC, the most common form of pancreatic cancer (and the type we are referring to throughout this conversation, though other, less common subtypes exist).

The stock surged after the announcement of two rare complete responses which were widely reported in the press.

Pancreatic cancer is projected to be the second most common cause of cancer deaths by 2030, not because it’s so common, but because it’s so lethal. Survival outcomes have not improved meaningfully in decades, even as other solid tumours have benefited from new therapies.

Curative surgery is possible in some early pre-metastatic cases, but symptoms usually only present when the cancer has progressed and chemotherapy is the only option – with limited benefit.

There’s an urgent need to improve the effectiveness of these treatments.

A key challenge is the tumour microenvironment. PDAC builds a dense, fibrotic stroma that raises pressure inside the tumour and physically blocks both drugs and immune cells from reaching where they need to be.  

This is where Amplia steps in, with their FAK inhibitor designed to loosen the fibrotic stroma and blunt resistance signalling, helping chemotherapy agents to infiltrate the tumour more effectively.

The program has FDA Fast Track status, and the company recently raised $27.5 million.

I hope you find the transcript below as interesting as I did.

Michael Frazis

Hi everyone, today I’m delighted to have the CEO of Amplia Therapeutics, Chris Burns, on the podcast to discuss the company and some of the exciting recent clinical results. Welcome, Chris.

Chris Burns

Hi, Michael. Glad to be here.

 Michael Frazis

Let’s start with the disease Amplia is focused on, pancreatic cancer. Could you explain how it develops, how it’s diagnosed, and why it’s been so challenging for clinicians to treat?

 Chris Burns

Pancreatic cancer affects an organ deep in the body, just below the stomach. Because of its location, it’s difficult to detect early. Most patients don’t experience symptoms until the disease is quite advanced.

More than half of patients are diagnosed when the cancer has already metastasized, spread to other parts of the body, making treatment extremely difficult. Metastatic pancreatic cancer has a five year survival of 13%, which is one of the, the lowest survivals of any cancer.

For patients diagnosed with metastatic disease, that number drops to around 3%. It’s one of the toughest cancers to treat, and survival outcomes remain very poor.

 Michael Frazis

So how do patients present? What are the key symptoms they'll have?

Is surgery usually the first option, if it's possible?

 Chris Burns

So, patients will often present with an array of different symptoms.

It can be as mild as back pain or altered bowel habit. It can be jaundice. It can indeed even be diagnosed after someone's been diagnosed with Type One diabetes.

Mild things, which often means it's diagnosed quite late.

One of the big challenges with pancreatic cancer is its trajectory.

By 2030, it’s predicted to become the second leading cause of cancer deaths worldwide. That’s partly because treatments for other cancers have improved, but also because incidence of pancreatic cancer itself is rising, especially in younger patients, even those just over 30.

So, if symptoms do appear, it’s critical they’re investigated promptly.

Michael Frazis

And what are the treatment options after diagnosis?

Chris Burns

It depends on whether the disease is metastatic. If it’s confined to the pancreas, surgery is usually the best option. But the pancreas is difficult to access surgically, and often the tumour is already too large to remove. In those cases, chemotherapy may be used for locally advanced disease.

There are also newer approaches.

For example, OncoSil Medical on the ASX is developing therapies for patients with unresectable, locally advanced pancreatic cancer. The goal is to shrink the tumour enough to make surgical removal possible.

So, in simple terms: early, localized disease may be treated with surgery; locally advanced disease is treated with a combination of chemotherapy and emerging therapies; but once the cancer is metastatic, treatment is largely limited to systemic chemotherapy. Radiation can be used when the disease is confined to the pancreas. But once it has spread, treatment is mainly chemotherapy. Around 75% of patients receive one of two regimens.

The first is gemcitabine plus nab-paclitaxel (Abraxane). These drugs are given in three weekly doses over a four-week cycle. This regimen is generally well tolerated, though it can cause long-term side effects. On average, it extends survival to around eight or nine months.

The other main option is FOLFIRINOX, a combination of four drugs given every two weeks. It’s more aggressive, harder to tolerate, and typically reserved for younger, fitter patients. Median survival with FOLFIRINOX is about 11 months which is slightly better than gemcitabine/Abraxane, but still poor overall.

Globally, both regimens are used. FOLFIRINOX is more common in the U.S., while in Australia gemcitabine/Abraxane is prescribed more often, largely because of the difference in intensity and side-effect profile.

Side effects vary. With gemcitabine/Abraxane, patients may develop cytopenias, a drop in blood cell counts due to gemcitabine, and peripheral neuropathy from Abraxane, where patients lose sensation in their fingers and toes. That can make simple tasks like eating or buttoning clothes very difficult. In fact, we’ve had trial patients come off treatment because of these toxicities.

FOLFIRINOX carries even more side effects such as nausea, fatigue, low blood counts and so is generally reserved for patients strong enough to handle it.

And unfortunately, that happens really, from the first dose onwards. It's a very challenging treatment.

Obviously, any way that we can then modify the aggressiveness of those treatments, maybe dial back some of the toxicity of the dose.

 Michael Frazis

Yeah. Difficult trade-off for the extra couple of months.

Why has pancreatic cancer been so difficult to treat? Why have survival rates not improved like they have in other solid tumours?

 Chris Burns

It's a good question.

One of the reasons is that pancreatic cancer is what we call a fibrotic tumour. If you look at the tumour tissue itself, it's very hard.

It's got this sort of scar tissue, this fibrous tissue that sits around it. It acts as a barrier essentially for any therapies that we might give patients or indeed even your immune system, your own immune cells can't really penetrate and get into the tumour and attack it.

So, you've got this fibrous surrounding tissue that's one major problem that leads to reduced immune attack.

It leads to difficulty when treating with chemotherapy.

 I've heard stories of people having the cancer detected, and by the time they go into surgery, which might be a couple of weeks, maybe a month later, the tumour's grown, substantially in that timeframe.

So, you do have a lot of different genetic drivers that are driving the tumour cells themselves to, to make it quite difficult to treat.

Michael Frazis

You mentioned the stroma, that fibrotic shell around the tumour. Is that one of the reasons why drugs have trouble penetrating and aren’t as effective as they are in other cancers?

Chris Burns

Exactly. Fibrosis is a response triggered by the cells surrounding the cancer, largely driven by inflammation.

That inflammatory environment stimulates fibrous tissue to form, which creates a dense barrier. It prevents chemotherapy, antibodies, and even immune cells from reaching the tumour effectively.

That’s a key challenge—and it’s where our drug comes in. It targets and inhibits FAK (focal adhesion kinase), a protein that contributes to the fibrotic process.

By doing so, the drug helps relax that dense tissue. It doesn’t remove it completely, but it loosens the barrier enough to allow better penetration of chemotherapy and immune cells into the tumour, increasing the chance of attacking the cancer directly.

Michael Frazis

That’s a good point to transition to FAK inhibitors and your drug specifically. You mentioned one mechanism already, can you explain the therapeutic hypothesis in more detail? How do you think it’s working?

Chris Burns

There are a couple of mechanisms at play. The first is the effect on the tumor microenvironment. By modulating the fibrotic tissue, we allow drugs and immune cells to penetrate more effectively. Normally, the body can mount an immune response against cancer cells, but that dense fibrous shield makes it very difficult.

The second mechanism is a direct effect on the cancer cells themselves. Our drug inhibits focal adhesion kinase, or FAK, a protein that is overexpressed in pancreatic cancer and drives cell survival, migration, and proliferation. By blocking FAK, we interfere with those processes and also block resistance pathways that often emerge in response to chemotherapy or targeted therapy. FAK activity is frequently upregulated when other drugs are used, so inhibiting it helps prevent resistance.

In short, it is a one-two punch. First, we weaken the tumor microenvironment to improve drug and immune penetration. Second, we target the cancer cells directly, reducing survival and blocking resistance.

Michael Frazis

Have FAK inhibitors been tried before, and what were the outcomes?

Chris Burns

FAK inhibitors have been around probably getting onto 20 years.

The very first-generation compounds weren't particularly selective or potent, and they had a lot of other issues.

All the preclinical data, the data in mouse models and other models, indicated that FAK inhibitors would work in pancreatic cancer.

A couple were taken into clinical studies, but because those drugs weren't particularly optimized, those early trials didn't work.

We became really interested in progressing our particular molecule.

We started the company Amplia here in Melbourne to commercialize a drug that was discovered at an industry academic partnership in Australia called the Cancer Therapeutics Cooperative Research Center.

This was a team of academics and industry people that came together around specific problems in drug discovery.

And one of them was developing inhibitors of FAK. We were aware of this drug. It was a very good drug in terms of the preclinical data that the team had developed, but it wasn't being taken into the clinic.

So, we started Amplia to develop this Australian drug in cancer. And we became interested in 2015 when there were some papers coming out for scientific literature showing that FAK inhibitors were very much involved in modulating the tumour microenvironment that hadn't really been appreciated up to that point.

Knowing of course, that pancreatic cancer has this fibrous shield, if you like, around the cancer. We thought moving the drug forward into the clinic with a particular focus in pancreatic cancer was a sensible thing to do.

So we teamed up with a very talented group of scientists at the Garvin Institute in Sydney who have a lot of expertise in pancreatic cancer, and particularly this fibrous tumour microenvironment.

That was Professor Paul Timson and his team. We worked with Paul and really showed that our drug did what we thought it should do in various models of pancreatic cancer.

With that data that we started the clinical program.

Michael Frazis

Thanks, it’s helpful to understand the background to FAK inhibition and why earlier approaches didn’t work so well. Why don’t we move on to your ACCENT trial. Can you run through the results now that you have them, what you were expecting, the threshold for success, and how the trial was designed?

Chris Burns

Absolutely. The ACCENT trial is still ongoing. It’s a study in metastatic pancreatic cancer where we combine our drug, AMP945 – which we now call narmafotinib, or “narma” for short – with chemotherapy. Patients take our drug orally in the days leading up to their chemotherapy, which consists of gemcitabine and Abraxane. Both of those drugs are reasonably well tolerated.

The trial began with a dose-escalation phase, where the goal was to find a dose that was both safe and well tolerated, while also providing sufficient FAK inhibition to deliver a therapeutic benefit.

That part of the trial was conducted a couple of years ago. We identified 400 milligrams as the right dose. It’s not especially high for an oral drug , it’s in line with many therapies of this type. Patients take it once daily as a pill in the morning.

Alongside that, they receive chemotherapy three times in each four-week cycle. The key question is whether our combination of narmafotinib with gemcitabine and Abraxane delivers better outcomes than the historical results for gemcitabine and Abraxane alone.

So, from the dose-escalation phase, we established 400 milligrams as the dose to take forward.

 At the beginning of 2024, we began recruiting patients. In total we enrolled 55 patients, with sites in both Australia and Korea. People often ask why Korea, and the reasons are clear. Korea has an outstanding healthcare system, excellent hospitals, and strong clinical trial capabilities. The teams there are also a pleasure to work with. In addition, the incidence of pancreatic cancer is slightly higher in Korea, which helps with recruitment.

Within just under 13 months, we completed enrolment of all 55 patients, finishing in mid-February this year. The trial has focused on monitoring the safety and tolerability of our drug in combination with gemcitabine and Abraxane, while also measuring efficacy.

When we compare our results against historical data for chemotherapy alone, the combination is performing better. For example, the confirmed objective response rate – meaning patients whose disease responded for at least two months – is 31 percent. That compares favourably with around 23 percent for gemcitabine and Abraxane alone.

Progression-free survival is also improved. Our figure, announced last month, was 7.6 months. That’s roughly two months longer than the five to six months typically seen with chemotherapy by itself. It may not sound like much, but in the context of metastatic pancreatic cancer, two months is very meaningful for patients.

We’re now seeing progression-free survival pushed out to seven to eight months. The really encouraging news, though, is what sits behind that single number. There’s a subset of patients doing exceptionally well. Seven patients have remained on the drug for more than 12 months, and two of them have now passed 18 months. That kind of prolonged disease control is very exciting in this setting.

So we’re seeing not only efficacy, but also durability, particularly in a subset of patients. Just as importantly, the addition of our drug to chemotherapy has not added a significant burden in terms of tolerability. Patients with pancreatic cancer already suffer side effects from the disease itself, such as vomiting, diarrhoea, and other gastrointestinal problems. Chemotherapy adds fatigue and nausea on top of that.

When we compare the incidence of side effects in our trial with historical data for chemotherapy alone, there’s no meaningful increase. Clinicians have also told us anecdotally that patients tolerate the combination well, and that the drug adds no additional burden. That’s a very positive outcome.

Michael Frazis

How should we interpret time on treatment? I think the median in our trial was just over 200 days, versus about 117 days in the historical benchmark. What does that actually tell us?

Chris Burns

That figure is a straightforward calculation. We look at when patients start and when they come off study. Most come off because their disease has progressed, typically meaning the tumor has grown by more than 20 percent from baseline. Some stop for non–tumor-related reasons, such as withdrawing consent, new symptoms, or other clinical issues. But progression is the main driver, whether that is pain, a new metastatic lesion, or simple tumor growth as resistance develops.

When we talk about median duration on trial, we are really asking how long patients can stay on treatment before they have to stop. In our July data cut, the median was 202 days, versus about 120 days for gemcitabine and Abraxane alone. That already looks meaningfully better.

Progression-free survival is more complex to calculate because it accounts for what happens both while patients are on study and after they come off. Our current estimate is 7.6 months, compared with about 5.5 months for gemcitabine and Abraxane.

Seventeen patients are still on study, so the dataset is ongoing and will evolve. We do not expect everyone to be off treatment for another six to nine months. Even so, the results so far are very encouraging across multiple measures.

Michael Frazis

There were two well-publicized complete responses. One was written up in the papers and got a lot of attention, which is great. But some people expected the median progression-free survival to improve by more than about two months. How do we square that?

How do we make sense of a small subset doing extremely well alongside a two-month median increase? And how might that translate to overall survival, which is ultimately what matters most?

Chris Burns

That’s right. We’re working to understand, at a molecular level, what distinguishes the tumours in patients who do very well from those who do not. We don’t have that answer yet, but it’s a key focus.

On the complete responses, they’re important because they’re very rare in metastatic pancreatic cancer. A complete response means all visible tumours on the routine CT scans, which are done every two months, disappear. Functionally, the patient appears cancer-free. We saw one such case among the 55 patients, which is already above what you’d expect historically.

The second highly publicized case was different. The patient still had a small lesion in the liver on imaging, so the medical team surgically examined it to confirm whether it was cancer. Pathology showed it wasn’t cancer, despite appearances on the scan. That is a pathological complete response, and it’s also extremely rare in metastatic pancreatic cancer.

Beyond those, we have other patients with very large tumour shrinkage who are staying on treatment for a long time. Across the cohort, some patients came off study quickly, while an estimated 25 percent are showing prolonged benefit on the combination. We need to tease out why that is, and what features of their cancer predict response to our drug plus chemotherapy.

This remains interim data. We still have patients on trial.

Michael Frazis

Got it.

But even if it if it's effective in a small subset, that's still quite compelling, right?

 Chris Burns

Particularly if we can identify what it is. Absolutely. Because then you can actually assess patients prior to treatment and enrich the patient group for those who are more likely to respond.

 That's this process of personalized medicine or, biomarker driven drug development.

We're talking with a number of groups both here in Australia and overseas, on how to tease apart the data sets we have and try and understand that it's not simple, but I think there's something there.

And we've got hints from some of the people we've been talking to that there is a molecular signature that we could hone in on. But nothing to speak about yet.

 Michael Frazis

What's the plan with FOLFIRINOX ?

I understand you're starting a trial, is it the same design but just using the different chemotherapy?

Chris Burns

There are a couple of differences. First, the chemotherapy is different. FOLFIRINOX is given once every 14 days, so roughly twice a month. Second, because our drug is well tolerated, patients will take it every day. That is simpler for patients than timing doses only around chemotherapy, which is what we do in the ACCENT study.

Looking ahead, because the drug appears active on its own and does not rely solely on chemotherapy, we are moving to daily dosing of narmafotinib together with FOLFIRINOX. This trial has opened in Australia, with sites in Sydney and Melbourne already recruiting, and the first patient has been enrolled. We have identified four sites in the United States. Activation there has been delayed by site paperwork, but we expect those centers to open shortly.

The study is being conducted under an Investigational New Drug application with the United States Food and Drug Administration. The FDA has reviewed the protocol, safety data, and the drug product and is comfortable with the submitted package.

This trial begins with a dose escalation, as ACCENT did. We expect to complete dose escalation in the first quarter of next year. FOLFIRINOX is more aggressive chemotherapy, so we need to determine how it affects safety and tolerability when combined with narmafotinib. Based on everything we have seen so far, we think the combination will be manageable. Our preclinical work gives us confidence that adding narmafotinib to FOLFIRINOX can improve outcomes, and now we aim to demonstrate that in patients.

Michael Frazis

When you think about timeline, you've still got those existing patients on the Accent trial, the FOLFIRINOX trial.

What's next?

Chris Burns

ACCENT should finish around the middle of 2026, based on our current pace. The investigator feedback has been very positive so far.

We are now planning a registration-enabling study of narmafotinib in combination with gemcitabine and Abraxane. That planning takes time, so we are starting the process now. We will go to the FDA shortly with detailed questions on the proposed design and seek guidance on whether our approach is appropriate. If the feedback is supportive, we will write the full protocol and begin engaging clinical partners in the United States, Australia, Korea, and other regions. The aim is to launch that registration study toward the end of 2026 if everything lines up. This would build on the same chemotherapy backbone used in ACCENT.

We already have FDA Fast Track designation for narmafotinib in advanced pancreatic cancer, which should help with timely interactions. While the FDA has been busy and timelines can shift, we are optimistic about productive engagement over the coming months.

In parallel, we are running the FOLFIRINOX combination trial. Sites in Sydney and Melbourne are open and recruiting, and U.S. sites are in the final stages of activation. This study is being conducted under our cleared IND, and we have the necessary ethics approvals. The goal is to show activity with both main first-line regimens in pancreatic cancer, since FOLFIRINOX is commonly preferred in the United States.

Because ACCENT started on gemcitabine and Abraxane, that is the regimen we expect to take into a pivotal, registration-quality trial first. We will then decide how best to advance the FOLFIRINOX combination, guided by the data as it comes through.

Michael Frazis

There have been positive results from other approaches in pancreatic cancer, like KRAS inhibitors. How do you see those fitting in, and is there an opportunity to partner if your drug helps turn cold tumours hot?

Are there any other combinations or partnerships you could pursue?

Chris Burns

Absolutely.

For a long time, pancreatic cancer was viewed as a very challenging area for drug development. That is changing. KRAS inhibitors are a newer class that target an oncogene mutated in many pancreatic tumours. Trial data to date are encouraging. Resistance does develop, and the side effects can be challenging, so most programs are being tested in second-line settings after chemotherapy. Whether they move into first-line treatment will depend on toxicity and response rates as more data emerge.

Our data, and what is in the scientific literature, suggest that combining a FAK inhibitor with a KRAS inhibitor can improve outcomes. By reducing fibrosis in the tumor microenvironment, more KRAS inhibitor can reach the tumor. At the same time, FAK inhibition can block resistance pathways that often emerge with KRAS inhibition. In other words, you get both better penetration and a direct effect on the cancer cells.

We see real potential in a FAK plus KRAS inhibitor combination. We are in early discussions with KRAS developers about combination studies to enhance efficacy and, potentially, allow slightly lower KRAS inhibitor dosing to help manage toxicity.

Michael Frazis

How does that work in practice?

Would you need to partner with another company to run the trial together, or would they run the trial, and you provide the drug?

Chris Burns

There's a number of different partnership models.

One is that we run the trial and secure access to their drug under a supply agreement. Another is a joint study where we share costs equally. These discussions are ongoing. We recently raised $27.5 million Australian dollars, primarily to support ACCENT and SIMPLICITY and to begin planning the registration study. A small portion is set aside for investigator initiated studies in pancreatic cancer that combine TIB with KRAS inhibitors.

We are in discussion with investigators, and through them with several KRAS developers. The goal is to test the combination, show added benefit, and potentially improve tolerability by enabling lower KRAS inhibitor doses. That would create another avenue for TIB, alongside improving outcomes with chemotherapy, to work in combination with KRAS inhibitors.

Another area worth noting is antibody drug conjugates. These are antibodies armed with a potent payload that binds a tumor antigen and delivers targeted chemotherapy. The challenge is that antibodies cannot easily reach the tumor if a fibrotic shield blocks entry. Because TIB can relax that fibrotic barrier, combinations with antibody drug conjugates in pancreatic cancer could be very promising. We are in active conversations on that front as well.

The longer term vision is that as new treatments come online, narmafotinib could serve as a maintenance style backbone that stays with patients through their treatment journey, improving the effectiveness of each therapy along the way. That is the goal.

Michael Frazis

How does it work commercially if your drug is used in combination? Are you able to comment on pricing, market size, and what that might look like in practice, particularly in combination settings?

Chris Burns

Combination pricing can be complex. The chemotherapy backbones we are using are generally inexpensive now. Gemcitabine is off patent, and the FOLFIRINOX components are generic. Abraxane is moving off exclusivity in many markets, though availability and pricing can vary by country.

We would be adding our oral small-molecule kinase inhibitor on top. In the United States, comparable targeted therapies are typically priced in the range of about 120,000 to 250,000 dollars per year. Our own pricing work suggests we could fit within that window, subject to standard market access and reimbursement processes.

If we co-develop with a patented asset such as a KRAS inhibitor, the commercial model would depend on the partner and jurisdiction. There is good precedent for reimbursement of combination regimens in oncology, but the exact structure would be worked through with the developer of the other asset.

Michael Frazis

And who's currently marketing those chemotherapy agents?

Chris Burns

Gemcitabine was originally marketed by Eli Lilly as Gemzar. Abraxane is marketed by Bristol Myers Squibb in many regions, and nab-paclitaxel generics are becoming available in some markets. FOLFIRINOX is a regimen made up of generic drugs, so there are multiple suppliers for its components.

In terms of innovator companies, more are moving into pancreatic cancer because it remains a large unmet need and the incidence is rising. With the right asset, there is a clear commercial opportunity.

 Michael Frazis

Got it. For the next readouts from ACCENT and SIMPLICITY, what survivability results would get the market, payers, and clinicians genuinely excited?

Chris Burns

So that's a great question.

Because metastatic pancreatic cancer is so devastating, even modest gains matter. The most recent U.S. approval in the first-line setting was the NALIRIFOX regimen, which combines liposomal irinotecan Onivyde with oxaliplatin, fluorouracil, and leucovorin. It was approved in 2024 and showed about a two-month improvement in median overall survival versus gemcitabine plus nab-paclitaxel. That was sufficient for approval and was welcomed by clinicians and advocacy groups.

Anything above a two-month overall survival improvement would be considered significant. Obviously, the larger the gain, the better. If we can pair a survival benefit with good tolerability, that strengthens the value proposition. And if we can identify biomarkers that predict who benefits most, we may be able to deliver an even larger improvement in selected patients. Work on that is ongoing.

Michael Frazis

Got it. So why don't we just take a high-level view of like, kind of the mid- and long-term plan here.

You've got to finish this current trial, you have the new trial with FOLFIRINOX, hopefully a registrational trial. And presumably though that will require either a partner or funding.

Are you able to take us through the midterm strategy over the next few years? 

Chris Burns

Near term, our priority is to complete the ACCENT trial and report overall survival. We expect to have a solid read by Q1 next year.

We will then refine the design of a registration-enabling study. We already have rough cost guidelines, but after our upcoming FDA interaction clarifies patient numbers and approach, we will engage clinical research organizations to price the trial in detail.

It is possible, given the quality of the data so far, that we partner with a pharma company to help run that study. If not, we will explore funding it with existing cash and, if needed, an additional raise later next year or into 2027, depending on how our funding evolves.

In parallel, we are pursuing regional licensing deals. This is a proven path for Australian biotechs and can provide upfront payments, milestones, and royalties. Because we are already running sites in Korea, there are clear opportunities there, and we are also exploring China.

Longer term, as we move toward a registration-enabling study, we will seek partners. As a small Australian biotech, we do not plan to market the drug ourselves. During and after the registration study, we will use data from ACCENT and from the SIMPLICITY trial to build relationships with potential pharma partners, with the goal of co-development or a license.

That is the model. The data to date have been encouraging, and we are seeing interest from business development teams at pharma and biotech companies globally and in our region. We will see where those discussions lead.

Michael Frazis

Is there anything that we've left out, or any key points that we should cover?

Chris Burns

Not at all. I think we’ve covered what we needed to. The opportunities we see for the molecule and the program are significant, and the data so far support our confidence that this is a good drug—safe, well tolerated, and enhancing the activity of chemotherapy.

We haven’t talked about other opportunities for narmafotinib. From the outset, we saw pancreatic cancer as one of several fibrotic tumours to explore. One of our competitors is the US company Verastem, which recently received FDA accelerated approval for its combination in low-grade serous ovarian cancer. We’ve had a lot of interest from ovarian cancer specialists about testing narmafotinib in that setting.

We do have to be disciplined and not spread ourselves too thin. If there is an opportunity to study narmafotinib in ovarian cancer through a charity or grant, we would jump at it. There are data from our work and from the literature suggesting that a FAK inhibitor in ovarian cancer has real potential.

So that is happening in the background as well. If there are developments, we will announce them to the market.

Michael Frazis

Okay, great to know. Well, why don't we wrap up there.

Thanks so much for coming on.

 Chris Burns

Thank you, Michael.

Appreciate the chance to talk and look forward to catching up again.